Nikola Curic

Evolving hypopituitarism as a consequence of traumatic brain injury (TBI) in childhood—call for attention

Hypopituitarism is a common complication of TBI in long-term survivors, more frequent than previously realized. It may be partial or complete, sometimes very subtle without visible lesions in hypothalamo-pituitary region and is diagnosed only by biochemical means. Neuroendocrine abnormalities caused by TBI may have significant implications for the recovery and rehabilitation of these patients. The subjects at risk are those who have suffered moderate to severe trauma, although mild intensity trauma may precede hypopituitarism also. Particular attention should be paid to this problem in children and adolescents. We describe a patient with hypopituitarism thought to be idiopathic due to mild head trauma which caused diabetes insipidus in childhood, gradual failure of pituitary hormones during the period of growth and development, and metabolic (dyslipidemia), physical (obesity), and cognitive impairments in the adult period.

Estimation of in vivo and in vitro exposure to bisphenol A as food contaminant

The goal of this cross-sectional study was to examine the occurrence of bisphenol A (BPA) in the morning spot urine taken from 145 female volunteers of various ages. Total urine BPA concentration was detected in 38.6% samples in the 0.92-70.96 μg/g Cr range. The majority of BPA + women belonged to the 25 + body mass index (BMI) group (54.5% were overweight and 43.4% were obese women). Occurrence of BPA in the urine samples was higher at 40 + ages. The maximum BPA concentration of 70.96 μg/g Cr was detected in the urine sample of an obese woman. It is known that BPA is highly toxic in vitro. In this study BPA impaired significantly the growth of all investigated cell lines, i.e. the EC50 values were reached at very low concentrations, in the range from 3.24 to 34.85 μg/mL. The obtained in vivo results suggest that a higher exposure to BPA could contribute to weight problems in women and the absence of the BPA in vitro selective toxicity studies indicates to its general toxic mode of action and raises awareness of the health risks associated with its ubiquitous presence in the environment.

Do diethyl phthalate (DEP) and di-2-ethylhexyl phthalate (DEHP) influence the metabolic syndrome parameters? Pilot study

The study objective was to determine if the healthy participants were exposed to diethyl phthalate (DEP) and di (2-ethylhexyl) phthalate (DEHP) and if this exposure could be linked to the development of metabolic syndrome. The study included 103 healthy volunteers of similar age with normal BMI values, waist circumference, total cholesterol, HDL, LDL, and triglycerides. DEP and DEHP were measured in the morning urine samples to detect monoethyl phthalate (MEP) and mono-2-ethylhexyl phthalate (MEHP). Two phthalate groups and a control group were formed. Both MEP group and control group had similar results. The correlations between MEP and the measured parameters were insignificant. The correlation between the MEHP group and the age was significantly negative, but between the MHEP group and the waist circumference the correlation was significantly positive. Lipids and lipoproteins were within the reference values and equal in both groups. The significant negative correlation was observed only between MEHP and HDL. Our population is exposed to DEP and DEHP. There was only a significant correlation between DEHP and the observed metabolic syndrome components. Its negative impact was higher as the participants were younger.

Relation between osteocalcin and the energy metabolism in obesity

Background/aims:Numerous findings have indicated the potential relation between the osteocalcin, the traditional parameter of bone turnover and the regulation of energy metabolism. The aim of this study was to identify the relationship between osteocalcin and calculated indexes, which evaluate insulin sensitivity, insulin resistance and/or secretory capacity of the pancreas, in non-diabetic, obese subjects. Methods:The study included 57 (11 men and 46 women) euglycemic, obese patients (BMI:41,03 ± 6,61kg/m2) and 48 healthy individuals, age and sex matched (BMI:23,15±2,04kg/m2). Plasma glucose and insulin levels during two hour oral glucose tolerance test (OGTT) were determined in order to calculate HOMA indexes (HOMA-IR, HOMA-B%), EISI (estimated insulin sensitivity index), EFP (estimated first phase) and ESP (estimated second phase). Osteocalcin was measured using Electrochemiluminescence (ECLIA) methodology. Results: Statistically lower osteocalcin was found in obese subjects (24.72±9.80 vs 33.31±10.89 ng/mL;p<0.01). Тhere was a statistically significant positive correlation between osteocalcin and EISI (r=0.340;p<0.01). The inverse correlations were found between the osteocalcin and HOMA-IR (r=-0.276;p<0.01), HOMA-B% (r=-0.337;p<0.01), EFP (r=-0.332;p<0.01) and ESP (r=-0.266;p<0.01). Multiple regression showed that, BMI and osteocalcin have a significant inverse prediction with EISI and HOMA-IR, but the level of prediction of BMI was is substantially higher. Conclusion: The effect of osteocalcin in the glyco-regulation is evident, but its contribution is significantly smaller in relation to primarily, obesity associated factors. Therefore, when assessing the position and the role in glycemic control, aways must bear in mind that osteocalcin represents only one of the many contributing factors, some of which exhibit dominant influence then osteocalcin itself.

Bone metabolism during substitution therapy of primary hypothyroidism

Introduction. The relation between thyroid hormones and bone metabolism markers in hyperthyroidism is well known. Earlier studies indicate the possibility of bone metabolism acceleration during the excessive replacement therapy with l-thyroxin in hypothyroid patients especially in one with other risk factors for bone metabolism impairment. This study evaluated the effect of physiological l-thyroxine treatment on bone metabolism in patient with primary hypothyroidism. Material and methods. In the study group of 30 hypothyroid patients individual thyroxine replacement was performed targeting euthyroid status. Bone and calcium metabolism parameters (osteocalcin-OC, alkaline phosphates-ALP, C-terminal cross-linking telopeptide type I-CL, parathormone-PTH, Ca, ionized Ca, P), thyroid hormone levels (T3, T4, TSH) were measured before treatment and when euthyroid status was achieved. Results and discussion. A significant treatment effect was observed for bone formation and resorption parameters before and during the therapy; OC (p=0.000024), CL (p=0.002648). Ionized calcium levels also showed significantly higher values in euthyroid status confirming bone metabolism acceleration during the l-thyroxine therapy (p= 0.020). Thus, calcium metabolism hormone regulators were not significantly different before and after the therapy; PTH (p=0.27). Thyroid hormone levels showed significant correlation with bone metabolism parameters before the therapy whereas this correlation was not found during therapy because of different individual l-thyroxine doses. Conclusion. It can be concluded that physiological doses of l-thyroxine therapy accelerate bone metabolism in hypothyroid patients. Thus, the argument against bone loss during physiological substitution is highly specific mutual correlation between bone formation and resorption parameters. These assumptions require further investigations in long term prospective studies in patients on replacement l-thyroxine therapy.